NUR 480 - NEURO: Questions With Correct
Solutions
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Terms in this set (221)
In the sympathetic nervous Norepinephrine
system, what does the -> adrenaline
neurotransmitter release?
what happens to the GI decreased GI motility
system in the sympathetic (d/t heart rate and other organs increasing.)
nervous system?
internal carotid arteries and vertebrobasilar arteries,
joined with posterior communicating arteries at base of
What is the Circle of Willis? brain.
*allows blood flow to the brain/through the brain
What happens if the Circle if arteries are blocked or interrupted, blood flow to the
of Willis is interrupted? brain is cut off which can result in a stroke.
*changes in LOC
-headache, constant, increased intensity w/no relief
-pupillary changes/impaired ocular movement
What are early signs of -increased drowsiness/lethargy
increased ICP? -restless w/o apparent cause (d/t brain
swelling/hemorrhage/tumor)
-agitation (w/o any apparent cause)
-N/V
, *projectile vomiting
-loss of corneal reflex (to test this -> place a cotton ball
on the corneal)
-VS changes -> cushing triad (increase systolic BP,
decreased HR, decreased RR) (d/t alternations in
cerebral perfusion, disease, trauma, swelling) - can lead
what are late s/s of to further destruction, immediate intervention is
increased intercranial important (ie. cerebral herniation)
pressure? -unilateral fixed and dilated pupil
-->ocular motor nerve is compressed (cranial nerve 3),
as the result of increased intracranial pressure (*doll
eyes*)
-->occurs as bottom portion of temporal lobe displaced
through tentorium cerebeli.
limited space in skull for expansion
-> compensation occurs
What is Monroe-Kellie
->displacing/shifting
Doctrine?
->increased absorption, decreased production of CSF
->decreased central blood volume
*our blood/brain/CSF volume will be consistently
shifting
(problem-when intrathoracic pressures are alternating
what can cause changes in
and this doesn't happen -> resulting in intracranial
altering intrathoracic
pressure rising)
pressure?
-coughing/sneezing
-straining or changing positions/posture
-change in BP/systemic CO2/O2 levels
-bulging fontanels
-cranial suture separation
s/s of infant ICP:
-increased head circumference
-high pitched cry
, *neuro assessments every 1-2 hours
->GCS (quick effective tool to determine the pt's neuro
status)
-assess LOC
-->cranial nerve function (pupil checks)
-->cerebellar function (balance/gait)
RN assessment for ICP:
-->sensory/motor function
-->reflexes (babinski)
-VS (closely monitor O2)
-maintain strict I & O -> fluid status will fluctuate
cerebral perfusion and pressure
-continuedly monitor cardiac rhythm
-cardiac markers (CBC/blood gas)
-serum electrolytes-> serum sodium
-serum osmolality (fluid status)
-BUN/creatine
-end tidal- CO2 continual monitoring to guide
Labs to monitor for ICP:
hyperventilation therapy during treatment for increased
ICP
-->hyperventilate to regulate/decrease whatever is
going on causing the ICP
-ABGs - assess metabolic state
-head CT -> can identify cause of ICP
ie)tumor/hematoma/hemorrhagic event or cerebral
diagnostic imaging for ICP: edema
-MRI
-transcranial doppler - assess cerebral blood flow
ICP> arterial blood pressure (ICP is HIGHER than
arterial BP)
-arteries collapse d/t ICP pressed against
-blood flow cut off -> losing highly nutrient O2/glucose
that the brain needs
what is compartment -cortical neurons, especially sensitive toO2 deficit (start
syndrome in the skull? to fail)
*vasomotor neurons markedly increase MAP during
ischemia in attempt to increase CPP ie)cushing triad
GOAL: increase MAP to increase cerebral perfusion
pressures by opening/reopening the collapsed artery
, a response to painful stimuli -
when pt neuros decline - pt
How is posturing related to
becomes unresponsive - body
ICP?
responds to pain w/abnormal
motor responses = posturing
caused by damage to the corticospinal tracts ->
typically seen in increased ICP
-Decorticate = Core (everything will be flexed inward,
what is decorticate towards the core)
posturing? --> arms adducted + flexed on chest, wrists and fingers
flexed on chest
--> legs extended, internally rotated
--> planter flexion of feet
damage to the brain stem
-arms adducted and extended -> at side, flexed out
what is decerebrate -wrists pronated, fingers flexed -> wrists bent, hands
posturing? outward makes an E shape
-legs extended
-planter flexion of feet
brain stem compression
-complication of ICP; can be caused by CCP - shifting
of brain tissue from an area of high pressure to an area
of lower pressure
what is cerebral herniation?
*whichever side brain shifts to, will cause more pressure
to that side of the brain
-->causing blood flow to stop
-->resulting in ischemia or brain death
-UNR/coma -> absence of motor and reflex responses
--> no spontaneous respirations (apnea)
--> no cephalic reflexes
manifestations of cerebral
-->isoelectric EEG
herniation:
-->apnea trial or flow study
*cushing's triad and +Babinski reflex -> will maintain
throughout
Solutions
Save
Terms in this set (221)
In the sympathetic nervous Norepinephrine
system, what does the -> adrenaline
neurotransmitter release?
what happens to the GI decreased GI motility
system in the sympathetic (d/t heart rate and other organs increasing.)
nervous system?
internal carotid arteries and vertebrobasilar arteries,
joined with posterior communicating arteries at base of
What is the Circle of Willis? brain.
*allows blood flow to the brain/through the brain
What happens if the Circle if arteries are blocked or interrupted, blood flow to the
of Willis is interrupted? brain is cut off which can result in a stroke.
*changes in LOC
-headache, constant, increased intensity w/no relief
-pupillary changes/impaired ocular movement
What are early signs of -increased drowsiness/lethargy
increased ICP? -restless w/o apparent cause (d/t brain
swelling/hemorrhage/tumor)
-agitation (w/o any apparent cause)
-N/V
, *projectile vomiting
-loss of corneal reflex (to test this -> place a cotton ball
on the corneal)
-VS changes -> cushing triad (increase systolic BP,
decreased HR, decreased RR) (d/t alternations in
cerebral perfusion, disease, trauma, swelling) - can lead
what are late s/s of to further destruction, immediate intervention is
increased intercranial important (ie. cerebral herniation)
pressure? -unilateral fixed and dilated pupil
-->ocular motor nerve is compressed (cranial nerve 3),
as the result of increased intracranial pressure (*doll
eyes*)
-->occurs as bottom portion of temporal lobe displaced
through tentorium cerebeli.
limited space in skull for expansion
-> compensation occurs
What is Monroe-Kellie
->displacing/shifting
Doctrine?
->increased absorption, decreased production of CSF
->decreased central blood volume
*our blood/brain/CSF volume will be consistently
shifting
(problem-when intrathoracic pressures are alternating
what can cause changes in
and this doesn't happen -> resulting in intracranial
altering intrathoracic
pressure rising)
pressure?
-coughing/sneezing
-straining or changing positions/posture
-change in BP/systemic CO2/O2 levels
-bulging fontanels
-cranial suture separation
s/s of infant ICP:
-increased head circumference
-high pitched cry
, *neuro assessments every 1-2 hours
->GCS (quick effective tool to determine the pt's neuro
status)
-assess LOC
-->cranial nerve function (pupil checks)
-->cerebellar function (balance/gait)
RN assessment for ICP:
-->sensory/motor function
-->reflexes (babinski)
-VS (closely monitor O2)
-maintain strict I & O -> fluid status will fluctuate
cerebral perfusion and pressure
-continuedly monitor cardiac rhythm
-cardiac markers (CBC/blood gas)
-serum electrolytes-> serum sodium
-serum osmolality (fluid status)
-BUN/creatine
-end tidal- CO2 continual monitoring to guide
Labs to monitor for ICP:
hyperventilation therapy during treatment for increased
ICP
-->hyperventilate to regulate/decrease whatever is
going on causing the ICP
-ABGs - assess metabolic state
-head CT -> can identify cause of ICP
ie)tumor/hematoma/hemorrhagic event or cerebral
diagnostic imaging for ICP: edema
-MRI
-transcranial doppler - assess cerebral blood flow
ICP> arterial blood pressure (ICP is HIGHER than
arterial BP)
-arteries collapse d/t ICP pressed against
-blood flow cut off -> losing highly nutrient O2/glucose
that the brain needs
what is compartment -cortical neurons, especially sensitive toO2 deficit (start
syndrome in the skull? to fail)
*vasomotor neurons markedly increase MAP during
ischemia in attempt to increase CPP ie)cushing triad
GOAL: increase MAP to increase cerebral perfusion
pressures by opening/reopening the collapsed artery
, a response to painful stimuli -
when pt neuros decline - pt
How is posturing related to
becomes unresponsive - body
ICP?
responds to pain w/abnormal
motor responses = posturing
caused by damage to the corticospinal tracts ->
typically seen in increased ICP
-Decorticate = Core (everything will be flexed inward,
what is decorticate towards the core)
posturing? --> arms adducted + flexed on chest, wrists and fingers
flexed on chest
--> legs extended, internally rotated
--> planter flexion of feet
damage to the brain stem
-arms adducted and extended -> at side, flexed out
what is decerebrate -wrists pronated, fingers flexed -> wrists bent, hands
posturing? outward makes an E shape
-legs extended
-planter flexion of feet
brain stem compression
-complication of ICP; can be caused by CCP - shifting
of brain tissue from an area of high pressure to an area
of lower pressure
what is cerebral herniation?
*whichever side brain shifts to, will cause more pressure
to that side of the brain
-->causing blood flow to stop
-->resulting in ischemia or brain death
-UNR/coma -> absence of motor and reflex responses
--> no spontaneous respirations (apnea)
--> no cephalic reflexes
manifestations of cerebral
-->isoelectric EEG
herniation:
-->apnea trial or flow study
*cushing's triad and +Babinski reflex -> will maintain
throughout
